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[PMID]:28742247
[Au] Autor:Zhiwei W; Yuan J; Yihui Y; Xin H; Jingtao C; Lei S; Yongjian D
[Ti] Título:Ventana immunohistochemistry assay for anaplastic lymphoma kinase gene rearrangement detection in patients with non-small cell lung cancer: A meta-analysis.
[So] Source:Thorac Cancer;8(5):471-476, 2017 Sep.
[Is] ISSN:1759-7714
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The aim of this study was to evaluate the diagnostic value of Ventana immunohistochemistry (IHC) assay for anaplastic lymphoma kinase (ALK) gene rearrangement screening in patients with non-small cell lung cancer (NSCLC). METHODS: Open published studies that reported the diagnostic performance of Ventana IHC assay for ALK gene rearrangement detection in NSCLC patients were extracted from PubMed, Embase, Google scholar, Wanfang, and China National Knowledge Infrastructure. The general information and number of true positive (tp), false positive (fp), false negative (fn), and true negative (tn) cases identified by Ventana IHC assay were extracted. The diagnostic sensitivity, specificity, positive likelihood ratio (+lr), negative likelihood ratio (-lr), diagnostic odds ratio (dor) and the summary receiver operating characteristic (ROC) curve were calculated using Stata 11.0 software. RESULTS: Ten studies, including 240 ALK positive and 1973 ALK negative NSCLC patients were included in this meta-analysis. The pooled diagnostic sensitivity, specificity, +lr, -lr, and dor were 0.94 (95% confidence interval [CI] 0.85-0.98), 1.00 (95% CI 0.99-1.00), 859.61 (95% CI 60.81-1200.00), 0.06 (95% CI 0.03-0.16), and 1400.00 (95% CI 813.29-23 000.00), respectively. The area under the ROC curve was 0.996 for Ventana IHC assay in detecting ALK gene rearrangement in NSCLC patients. CONCLUSION: The sensitivity and specificity of Ventana IHC assay for the detection of ALK gene rearrangement were high, thus Ventana IHC could substitute fluorescence in situ hybridization for the screening of ALK+ NSCLC patients.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Rearranjo Gênico
Neoplasias Pulmonares/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Carcinoma Pulmonar de Células não Pequenas/genética
Seres Humanos
Imuno-Histoquímica/métodos
Neoplasias Pulmonares/genética
Proteínas de Fusão Oncogênicas/metabolismo
Curva ROC
Receptores Proteína Tirosina Quinases/genética
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Oncogene Proteins, Fusion); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (anaplastic lymphoma kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1111/1759-7714.12468


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Registro de Ensaios Clínicos
Registro de Ensaios Clínicos
Registro de Ensaios Clínicos
Registro de Ensaios Clínicos
Registro de Ensaios Clínicos
Registro de Ensaios Clínicos
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[PMID]:29466156
[Au] Autor:Drilon A; Laetsch TW; Kummar S; DuBois SG; Lassen UN; Demetri GD; Nathenson M; Doebele RC; Farago AF; Pappo AS; Turpin B; Dowlati A; Brose MS; Mascarenhas L; Federman N; Berlin J; El-Deiry WS; Baik C; Deeken J; Boni V; Nagasubramanian R; Taylor M; Rudzinski ER; Meric-Bernstam F; Sohal DPS; Ma PC; Raez LE; Hechtman JF; Benayed R; Ladanyi M; Tuch BB; Ebata K; Cruickshank S; Ku NC; Cox MC; Hawkins DS; Hong DS; Hyman DM
[Ad] Endereço:From Memorial Sloan Kettering Cancer Center (A. Drilon, J.F.H., R.B., M.L., D.M.H.) and Weill Cornell Medical College (A. Drilon, D.M.H.), New York; University of Texas Southwestern Medical Center-Children's Health, Dallas (T.W.L.); Stanford Cancer Center, Stanford University, Palo Alto (S.K.), Chil
[Ti] Título:Efficacy of Larotrectinib in TRK Fusion-Positive Cancers in Adults and Children.
[So] Source:N Engl J Med;378(8):731-739, 2018 02 22.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Fusions involving one of three tropomyosin receptor kinases (TRK) occur in diverse cancers in children and adults. We evaluated the efficacy and safety of larotrectinib, a highly selective TRK inhibitor, in adults and children who had tumors with these fusions. METHODS: We enrolled patients with consecutively and prospectively identified TRK fusion-positive cancers, detected by molecular profiling as routinely performed at each site, into one of three protocols: a phase 1 study involving adults, a phase 1-2 study involving children, or a phase 2 study involving adolescents and adults. The primary end point for the combined analysis was the overall response rate according to independent review. Secondary end points included duration of response, progression-free survival, and safety. RESULTS: A total of 55 patients, ranging in age from 4 months to 76 years, were enrolled and treated. Patients had 17 unique TRK fusion-positive tumor types. The overall response rate was 75% (95% confidence interval [CI], 61 to 85) according to independent review and 80% (95% CI, 67 to 90) according to investigator assessment. At 1 year, 71% of the responses were ongoing and 55% of the patients remained progression-free. The median duration of response and progression-free survival had not been reached. At a median follow-up of 9.4 months, 86% of the patients with a response (38 of 44 patients) were continuing treatment or had undergone surgery that was intended to be curative. Adverse events were predominantly of grade 1, and no adverse event of grade 3 or 4 that was considered by the investigators to be related to larotrectinib occurred in more than 5% of patients. No patient discontinued larotrectinib owing to drug-related adverse events. CONCLUSIONS: Larotrectinib had marked and durable antitumor activity in patients with TRK fusion-positive cancer, regardless of the age of the patient or of the tumor type. (Funded by Loxo Oncology and others; ClinicalTrials.gov numbers, NCT02122913 , NCT02637687 , and NCT02576431 .).
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Neoplasias/tratamento farmacológico
Pirazóis/uso terapêutico
Pirimidinas/uso terapêutico
Receptores Proteína Tirosina Quinases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Criança
Pré-Escolar
Intervalo Livre de Doença
Feminino
Seres Humanos
Lactente
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Neoplasias/química
Proteínas de Fusão Oncogênicas/análise
Proteínas Quinases/análise
Proteínas Quinases/genética
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ARRY-470); 0 (Antineoplastic Agents); 0 (Oncogene Proteins, Fusion); 0 (Pyrazoles); 0 (Pyrimidines); EC 2.7.- (Protein Kinases); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.11.28 (tropomyosin kinase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1714448


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[PMID]:28464908
[Au] Autor:Chia SK; Ellard SL; Mates M; Welch S; Mihalcioiu C; Miller WH; Gelmon K; Lohrisch C; Kumar V; Taylor S; Hagerman L; Goodwin R; Wang T; Sakashita S; Tsao MS; Eisenhauer E; Bradbury P
[Ad] Endereço:Medical Oncology, British Columbia Cancer Agency (BCCA), Vancouver, BC, Canada. schia@bccancer.bc.ca.
[Ti] Título:A phase-I study of lapatinib in combination with foretinib, a c-MET, AXL and vascular endothelial growth factor receptor inhibitor, in human epidermal growth factor receptor 2 (HER-2)-positive metastatic breast cancer.
[So] Source:Breast Cancer Res;19(1):54, 2017 May 02.
[Is] ISSN:1465-542X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The mechanisms of resistance to anti-human epidermal growth factor receptor 2 (HER 2) therapies are unclear but may include the tyrosine-protein kinase Met (c-Met), vascular endothelial growth factor (VEGF) and AXL pathways. Foretinib is an inhibitor of c-Met, VEGF receptor 2 (VEGFR-2), platelet-derived growth factor receptor beta (PDGFRB), AXL, Fms-like tyrosine kinase 3 (FLT3), angiopoiten receptor (TIE-2), RET and RON kinases. This phase Ib study sought to establish the associated toxicities, pharmacokinetics (PK) and recommended phase II doses (RP2D) of foretinib and lapatinib in a cohort of HER-2-positive patients with metastatic breast cancer (MBC). METHODS: Women with HER-2 positive MBC, Performance status (PS 0-2), and no limit on number of prior chemotherapies or lines of anti-HER-2 therapies were enrolled. A 3 + 3 dose escalation design was utilized. Four dose levels were intended with starting doses of foretinib 30 mg and lapatinib 750 mg orally once a day (OD) on a 4-weekly cycle. Assessment of c-MET status from the primary archival tissue was performed. RESULTS: We enrolled 19 patients, all evaluable for toxicity assessment and for response evaluation. Median age was 60 years (34-86 years), 95% were PS 0-1, 53% were estrogen receptor-positive and 95% had at least one prior anti-HER-2-based regimen. The fourth dose level was reached (foretinib 45 mg/lapatinib 1250 mg) with dose-limiting toxicities of grade-3 diarrhea and fatigue. There was only one grade-4 non-hematological toxicity across all dose levels. There were no PK interactions between the agents. A median of two cycles was delivered across the dose levels (range 1-20) with associated progression-free survival of 3.2 months (95% CI 1.61-4.34 months). By immunohistochemical assessment with a specified cutoff, none of the 17 samples tested were classified as positive for c-Met. CONCLUSIONS: The RP2D of the combined foretinib and lapatinib is 45 mg and 1000 mg PO OD, respectively. Limited activity was seen with this combination in a predominantly unselected cohort of HER-2-positive patients with MBC.
[Mh] Termos MeSH primário: Anilidas/administração & dosagem
Neoplasias da Mama/tratamento farmacológico
Inibidores de Proteínas Quinases/administração & dosagem
Quinazolinas/administração & dosagem
Quinolinas/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Intervalo Livre de Doença
Feminino
Seres Humanos
Meia-Idade
Metástase Neoplásica
Proteínas Proto-Oncogênicas/antagonistas & inibidores
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas c-met/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-met/genética
Receptores Proteína Tirosina Quinases/antagonistas & inibidores
Receptores Proteína Tirosina Quinases/genética
Receptor ErbB-2/genética
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/genética
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (GSK 1363089); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins); 0 (Quinazolines); 0 (Quinolines); 0VUA21238F (lapatinib); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (MET protein, human); EC 2.7.10.1 (Proto-Oncogene Proteins c-met); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1); EC 2.7.10.1 (axl receptor tyrosine kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s13058-017-0836-3


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[PMID]:29288940
[Au] Autor:Geng K; Xia Z; Ji Y; Zhang RR; Sun D; Ai J; Song Z; Geng M; Zhang A
[Ad] Endereço:CAS Key Laboratory of Receptor Research and the State Key Laboratory for Drug Research, Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences, Shanghai 201203, China; University of Chinese Academy of Sciences, NO.19A Yuquan Road, Beijing 100049, China.
[Ti] Título:Discovery of 2,4-diarylaminopyrimidines bearing a resorcinol motif as novel ALK inhibitors to overcome the G1202R resistant mutation.
[So] Source:Eur J Med Chem;144:386-397, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:To address drug resistance caused by ALK kinase mutations, especially the most refractory and predominant mutation G1202R for the second-generation ALK inhibitor, a series of new diarylaminopyrimidine analogues were designed by incorporating a resorcinol moiety (A-ring) to interact the ALK kinase domain where the G1202R is located. Compound 12d turns out as the most potent with IC values of 1.7, 3.5, and 1.8 nM against ALK wild type, gatekeeper mutant L1196M, and the G1202R mutant, respectively. More importantly, compound 12d has excellent inhibitory effects against the proliferation of BaF3 cells specifically expressing ALK wild type, gatekeeper L1196M, and the most challenging mutant G1202R, with IC values all less than 1.5 nM. Collectively, compound 12d is worthy of further investigation as a new more potent third-generation ALK inhibitor to circumvent drug resistance of both the first-generation and the second-generation inhibitors.
[Mh] Termos MeSH primário: Descoberta de Drogas
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
Receptores Proteína Tirosina Quinases/antagonistas & inibidores
Resorcinóis/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Seres Humanos
Simulação de Acoplamento Molecular
Estrutura Molecular
Mutação
Inibidores de Proteínas Quinases/síntese química
Inibidores de Proteínas Quinases/química
Pirimidinas/síntese química
Pirimidinas/química
Receptores Proteína Tirosina Quinases/genética
Receptores Proteína Tirosina Quinases/metabolismo
Resorcinóis/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (Resorcinols); 109-12-6 (2-aminopyrimidine); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (anaplastic lymphoma kinase); YUL4LO94HK (resorcinol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


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[PMID]:29233871
[Au] Autor:Fraser J; Cabodevilla AG; Simpson J; Gammoh N
[Ad] Endereço:Cancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, U.K.
[Ti] Título:Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking.
[So] Source:Essays Biochem;61(6):597-607, 2017 12 12.
[Is] ISSN:1744-1358
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Vesicular trafficking events play key roles in the compartmentalization and proper sorting of cellular components. These events have crucial roles in sensing external signals, regulating protein activities and stimulating cell growth or death decisions. Although mutations in vesicle trafficking players are not direct drivers of cellular transformation, their activities are important in facilitating oncogenic pathways. One such pathway is the sensing of external stimuli and signalling through receptor tyrosine kinases (RTKs). The regulation of RTK activity by the endocytic pathway has been extensively studied. Compelling recent studies have begun to highlight the association between autophagy and RTK signalling. The influence of this interplay on cellular status and its relevance in disease settings will be discussed here.
[Mh] Termos MeSH primário: Autofagia/fisiologia
Endocitose/fisiologia
Receptores Proteína Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Animais
Autofagia/genética
Endocitose/genética
Seres Humanos
Neoplasias/genética
Neoplasias/metabolismo
Receptores Proteína Tirosina Quinases/genética
Transdução de Sinais/genética
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1042/EBC20170091


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[PMID]:28470860
[Au] Autor:Hong Y; Zisimopoulou P; Trakas N; Karagiorgou K; Stergiou C; Skeie GO; Hao HJ; Gao X; Owe JF; Zhang X; Yue YX; Romi F; Wang Q; Li HF; Gilhus NE; Tzartos SJ
[Ad] Endereço:Department of Clinical Medicine, University of Bergen, Bergen, Norway.
[Ti] Título:Multiple antibody detection in 'seronegative' myasthenia gravis patients.
[So] Source:Eur J Neurol;24(6):844-850, 2017 Jun.
[Is] ISSN:1468-1331
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Myasthenia gravis (MG) is an autoimmune disease caused by antibody mediated impairment in the neuromuscular junction. Seronegative MG (SNMG) without antibodies against acetylcholine receptor (AChR) and muscle-specific kinase (MuSK) by routine assays accounts for about 20% of all MG patients. METHODS: Plasma from 81 Chinese MG patients previously found to be seronegative was tested by routine assays for AChR and MuSK antibodies. These samples were screened by (i) a novel, highly sensitive radioimmunoassay for AChR antibodies; (ii) cell-based assays for clustered AChR, MuSK and lipoprotein receptor-related protein 4 (LRP4) antibodies; (iii) a radioimmunoassay for titin antibodies. RESULTS: Antibodies to AChR, MuSK, LRP4 and titin were found in 25% (20/81), 4% (3/81), 7% (6/81) and 6% (5/78) of SNMG patients, respectively. In total, 37% of SNMG patients were found to be positive for at least one of the tested antibodies. AChR antibody positive patients had more severe disease (P = 0.008) and a trend towards fewer remissions/minimal manifestations than AChR antibody negative patients. The four patients with coexistence of antibodies had more severe disease, whilst the seronegative patients had milder MG (P = 0.015). CONCLUSIONS: Detection of multiple muscle antibodies by more sensitive assays provides additional information in diagnosing and subgrouping of MG and may guide MG treatment.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Conectina/imunologia
Proteínas Relacionadas a Receptor de LDL/imunologia
Miastenia Gravis/imunologia
Receptores Proteína Tirosina Quinases/imunologia
Receptores Colinérgicos/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
Miastenia Gravis/sangue
Radioimunoensaio
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Connectin); 0 (LDL-Receptor Related Proteins); 0 (LRP4 protein, human); 0 (Receptors, Cholinergic); 0 (TTN protein, human); EC 2.7.10.1 (MUSK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/ene.13300


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[PMID]:29372799
[Au] Autor:Andreenkova OV; Adonyeva NV; Eremina MA; Gruntenko NE; Rauschenbach IY
[Ti] Título:The insulin-like receptor gene expression in the tissues synthesizing gonadotropic hormones at sexual maturation of Drosophila melanogaster females].
[So] Source:Genetika;52(11):1342-4, 2016 Nov.
[Is] ISSN:0016-6758
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng; rus
[Ab] Resumo:The insulin/insulin-like growth factor signaling pathway is involved in the regulation of the synthesis of insect gonadotropic hormones, juvenile (JH) and 20-hydroxyecdysone (20E). We carried out the immunohistochemical analysis of the insulin receptor (InR) expression in the corpus allatum (the JH-producing gland) and in the ovarian follicular cells (a site for the synthesis of 20E precursor, ecdysone) in the process of sexual maturation of D. melanogaster females and examined the influence of exogenous JH on the InR expression in these tissues. For the first time, it was demonstrated that InR was expressed in follicular cells and that its expression in corpus allatum and follicular cells of Drosophila females was stage-specific, i.e., the expression intensity in young females greatly exceeded that in mature individuals. We also found a negative feedback loop in the regulation of JH levels by the insulin signaling pathway in Drosophila adults: the experimental increase in the JH titers in young females dramatically reduced the InR expression intensity in corpus allatum and follicular cells.
[Mh] Termos MeSH primário: Proteínas de Drosophila/biossíntese
Regulação da Expressão Gênica/fisiologia
Hormônios Juvenis/metabolismo
Ovário/metabolismo
Receptores Proteína Tirosina Quinases/biossíntese
Maturidade Sexual/fisiologia
[Mh] Termos MeSH secundário: Animais
Drosophila melanogaster
Feminino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Juvenile Hormones); EC 2.7.10.1 (InR protein, Drosophila); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE


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[PMID]:29173772
[Au] Autor:Tian HX; Zhang XC; Yang JJ; Guo WB; Chen ZH; Wang Z; Wu YL
[Ad] Endereço:Medical Research Center, Guangdong Lung Cancer Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China.
[Ti] Título:Clinical characteristics and sequence complexity of anaplastic lymphoma kinase gene fusions in Chinese lung cancer patients.
[So] Source:Lung Cancer;114:90-95, 2017 Dec.
[Is] ISSN:1872-8332
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To investigate the clinical characteristics of anaplastic lymphoma kinase (ALK) rearrangements and sequence complexity of the ALK fusion gene in Chinese lung cancer patients. METHODS: We prospectively screened ALK rearrangements in 1474 lung cancer specimens, including 1387 cases of non-small cell lung cancer (NSCLC), 54 cases of small cell lung cancer (SCLC), and 33 cases of cancer with lung metastasis from other organs by both standard polymerase chain reaction (PCR) and rapid amplification of cDNA ends (RACE)-coupled PCR. Fifteen cases of ALK-positive RACE-coupled PCR products were transformed into Escherichia coli for molecular cloning and sequenced for complexity analysis. RESULTS: The overall frequency of ALK rearrangements was 5.1% (71/1387) in NSCLC. In 71 positive cases, the coexistence of epidermal growth factor receptor (EGFR) and ALK variations was found in 6 cases (8.5%), and the coexistence of different ALK variants was found in 2 cases (2.8%) (1 case with variants 1 and 9; the other case with variants 3 and 2) by PCR analysis. Furthermore, through sequence cloning analysis of 15 cases of non-selective ALK-positive samples, two cases with variants 1 and 3 harbored the coexistence of three subtypes (variant 1 subtypes: E13; A20, E13del63; A20 and E7E12E13; A20 and variant 3 subtypes: E6; A20, E6ins33; A20 and E3E6; A20). Variant 3a and 3b subtypes were always coexistent and had the same proportion of ALK variant 3 rearrangements. ALK rearrangement was associated with young age, female gender, never-smokers, those with adenocarcinoma, advanced stage, and EGFR mutations. No ALK fusion was detected in 54 cases of SCLC or 33 cases of cancer with lung metastasis from other organs. CONCLUSIONS: The identification of novel ALK variants, the coexistence of EGFR mutations and ALK fusions, the coexistence of ALK variants, and the coexistence of subtypes reveal the diversity and sequence complexity of ALK fusions.
[Mh] Termos MeSH primário: Grupo com Ancestrais do Continente Asiático/genética
Carcinoma Pulmonar de Células não Pequenas/genética
Fusão Gênica/genética
Neoplasias Pulmonares/genética
Receptores Proteína Tirosina Quinases/genética
Carcinoma de Pequenas Células do Pulmão/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/patologia
Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma Pulmonar de Células não Pequenas/patologia
Feminino
Variação Genética/genética
Variação Estrutural do Genoma/genética
Seres Humanos
Neoplasias Pulmonares/patologia
Neoplasias Pulmonares/secundário
Masculino
Meia-Idade
Terapia de Alvo Molecular/métodos
Estudos Prospectivos
Receptor do Fator de Crescimento Epidérmico/genética
Carcinoma de Pequenas Células do Pulmão/patologia
Fumar/epidemiologia
Fumar/tendências
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.1 (anaplastic lymphoma kinase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:29269528
[Au] Autor:Zinzani PL
[Ad] Endereço:UNIVERSITY OF BOLOGNA.
[Ti] Título:ALCL: is it now a curable disease?
[So] Source:Blood;130(25):2691-2692, 2017 12 21.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Doença de Hodgkin
Linfoma Anaplásico de Células Grandes
[Mh] Termos MeSH secundário: Seres Humanos
Proteínas Tirosina Quinases
Receptores Proteína Tirosina Quinases
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-10-811083


  10 / 15561 MEDLINE  
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[PMID]:29253861
[Au] Autor:Eich G; Bartosova M; Tischer C; Wlodkowski TT; Schaefer B; Pichl S; Kraewer N; Ranchin B; Vondrak K; Liebau MC; Hackert T; Schmitt CP
[Ad] Endereço:Center for Pediatric and Adolescent Medicine, University Hospital Heidelberg, Heidelberg, Germany.
[Ti] Título:Bicarbonate buffered peritoneal dialysis fluid upregulates angiopoietin-1 and promotes vessel maturation.
[So] Source:PLoS One;12(12):e0189903, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ultrafiltration decline is a progressive issue for patients on chronic peritoneal dialysis (PD) and can be caused by peritoneal angiogenesis induced by PD fluids. A recent pediatric trial suggests better preservation of ultrafiltration with bicarbonate versus lactate buffered fluid; underlying molecular mechanisms are unknown. METHODS: Angiogenic cytokine profile, tube formation capacity and Receptor Tyrosine Kinase translocation were assessed in primary human umbilical vein endothelial cells following incubation with bicarbonate (BPDF) and lactate buffered (LPDF), pH neutral PD fluid with low glucose degradation product content and lactate buffered, acidic PD fluid with high glucose degradation product content (CPDF). Peritoneal biopsies from age-, PD-vintage- and dialytic glucose exposure matched, peritonitis-free children on chronic PD underwent automated histomorphometry and immunohistochemistry. RESULTS: In endothelial cells angiopoietin-1 mRNA and protein abundance increased 200% upon incubation with BPDF, but decreased by 70% with LPDF as compared to medium control; angiopoietin-2 remained unchanged. Angiopoietin-1/Angiopoietin-2 protein ratio was 15 and 3-fold increased with BPDF compared to LPDF and medium. Time-lapse microscopy with automated network analysis demonstrated less endothelial cell tube formation with BPDF compared to LPDF and CPDF incubation. Receptor Tyrosine Kinase translocated to the cell membrane in BPDF but not in LPDF or CPDF incubated endothelial cells. In children dialyzed with BPDF peritoneal vessels were larger and angiopoietin-1 abundance in CD31 positive endothelium higher compared to children treated with LPDF. CONCLUSION: Bicarbonate buffered PD fluid promotes vessel maturation via upregulation of angiopoietin-1 in vitro and in children on dialysis. Our findings suggest a molecular mechanism for the observed superior preservation of ultrafiltration capacity with bicarbonate buffered PD fluid with low glucose degradation product content.
[Mh] Termos MeSH primário: Angiopoietina-1/metabolismo
Bicarbonatos/química
Tampões (Química)
Diálise Peritoneal
[Mh] Termos MeSH secundário: Adolescente
Angiopoietina-2/metabolismo
Biópsia
Criança
Doença Crônica
Citocinas/metabolismo
Células Endoteliais/metabolismo
Glucose/química
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Concentração de Íons de Hidrogênio
Nefropatias/terapia
Lactatos/química
Peritônio/patologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANGPT1 protein, human); 0 (ANGPT2 protein, human); 0 (Angiopoietin-1); 0 (Angiopoietin-2); 0 (Bicarbonates); 0 (Buffers); 0 (Cytokines); 0 (Lactates); 0 (Platelet Endothelial Cell Adhesion Molecule-1); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189903



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